Field of the Invention
The present invention relates to implantable medical devices and methods, and more particularly, to an implantable pacemaker that automatically adapts its atrial-ventricular (AV) delay to maximize the cardiac output for patients having a cardiomyopathy.
The heart is a pump that pumps life-sustaining blood throughout the body of the patient. The human heart comprises a left side and a right side, with each side having a first chamber, known as the atrium, and a second chamber, known as the ventricle. The atrium receives blood returning from other body locations. At an appropriate time, determined by the sinoatrial (SA) node, an electrical stimulus is provided that causes the muscle tissue surrounding the atrium to depolarize. Depolarization of the atrial muscle tissue is manifest by the occurrence of an electrical signal known as the P-wave. Immediately following the P-wave, the atrial muscle tissue physically contracts, forcing the blood held in the atrium through a one-way valve into the ventricle. The SA node stimulus that caused the atrium to depolarize also travels to the ventricle through the atrioventricular (AV) node and the atrioventricular (AV) bundle. The AV node is a mass of modified heart muscle situated in the lower middle part of the right atrium. It receives the impulse to contract from the sinoatrial node, via the atria, and transmits it through the atrioventricular bundle to the ventricles. The AV bundle is a bundle of modified heart muscle fibers (Purkinje fibers) that pass from the AV node forward to the septum between the ventricles, where it divides into right and left bundles, one for each ventricle. The fibers thus transmit the SA node stimulus from the atria, via the AV node, to the ventricles. However, as the SA node stimulus travels through the AV bundle, it is delayed by an amount commensurate with the same time it takes the blood to physically flow from the atrium to the ventricle.
After the delay through the AV bundle, which delay may be referred to as the natural conduction time of the heart, the SA node stimulus arrives at the ventricular muscle tissue, causing it to depolarize. Depolarization of the ventricular muscle tissue is manifest by the occurrence of an electrical signal known as the R-wave (sometimes referred to as the QRS complex). Immediately following the R-wave, the ventricular muscle tissue physically contracts, forcing the blood held therein through one or more arteries to various body locations. In this manner, then, the heart "beats" or pumps blood by having the atria contract at a rate determined by the SA node, and after the natural conduction time, by having the ventricles contract. After a longer delay, when the atrium has refilled with blood returning from throughout the body, the process repeats.
The heart of a typical healthy patient may beat 60-70 times per minute when the patient is at rest. When the patient is undergoing significant physiological stress, as occurs, e.g., during physical exercise, the rate at which the heart beats, the "heart rate," increases significantly, e.g, up to 150-170 times per minute. The above-described process wherein the atria and ventricles sequentially depolarize and contract in order to pump blood, and get ready to depolarize again, is referred to herein as the "cardiac cycle." A given cardiac cycle thus includes one R-wave (or equivalent ventricular activity evidencing depolarization of the ventricles) and one P-wave (or equivalent atrial activity evidencing depolarization of the atria). The length of the cardiac cycle (which represents the period of the heart rate) may be measured as the time interval between successive P-waves or R-waves, although R-waves are usually used because they are easier to detect.
A pacemaker is an implantable medical device that monitors the activity of the heart for the occurrence of P-waves and/or R-waves, and steps in with electronically generated stimuli, when needed, to force the depolarization of the atria and/or ventricles. A pacemaker-generated stimulus that is delivered to the atrium is referred to herein as an "A-pulse." A pacemaker-generated stimulus that is delivered to the ventricle is referred to herein as a "V-pulse." Most pacemakers are configured to provide an A-pulse and/or V-pulse only if a prescribed period of time has elapsed without the occurrence of a P-wave and/or an R-wave, i.e., without the occurrence of natural heart beats.
The prescribed period of time used by the pacemaker between contraction of the ventricle and contraction of the atrium is generally referred to as the V-A Interval, or the atrial escape interval. For most dual-chamber pacemaker modes of operation, only if a P-wave does not occur during the atrial escape interval will the pacemaker step in at the conclusion of such interval and generate an A-pulse.
The prescribed period of time used by the pacemaker between contraction of the atrium and contraction of the ventricle is referred to as the A-V Interval, or sometimes it is called the "AV Delay." The pacemaker, for most dual-chamber modes of operation, generates a V-pulse only if the AV Delay elapses without the occurrence of an R-wave.
In the above-described manner, the heart is thus afforded as much time as possible to beat on its own before the electronically-generated stimuli of the pacemaker are delivered to the heart, causing it to beat at the rate set by the pacemaker.
Heretofore, most cardiac patients using a pacemaker have suffered from at least one of various cardiac conditions or diseases that affect either the ability of the SA node to maintain and sustain a satisfactory heart beat rate (hereafter "rate problems"), or the ability of the AV node or the AV bundle to conduct a suitable stimulus to the ventricle (hereafter "conduction problems"). Advantageously, both rate problems and conduction problems lend themselves well to a pacemaker solution because the underlying cardiac muscle tissue is in place and is capable of responding to the electronically-generated stimuli produced by the pacemaker.
Unfortunately, there remain a significant number of patients that suffer from one or more conditions that cannot be characterized as either rate problems or conduction problems. One such problem is known as hypertrophic cardiomyopathy. Another is known as dilated cardiomyopathy. While there are medical or clinical differences between these two forms of cardiomyopathy, for purposes of the present invention they may be considered the same problem, and will be referred to hereafter as simply "cardiomyopathy."
In general, a patient suffering from cardiomyopathy experiences a significant reduction in cardiac output because the heart muscle is unable to perform its function of contracting in response to the SA node stimulus. By "cardiac output," it is meant the ability of the heart to efficiently pump blood. Thus, a patient suffering from cardiomyopathy will generally not have as much blood pumped per heart beat (stroke volume) as may be needed. Cardiomyopathy patients are referred to as being moderately to severely symptomatic of low cardiac output syndrome. The only treatment for low cardiac output syndrome, up to now, has been heart transplantation. Disadvantageously, heart transplantation is not a viable solution for most patients. Not only are hearts suitable for transplant difficult and expensive to secure, but even when secured, a very dangerous and complicated surgery must follow in order to successfully perform the transplantation operation. What is thus needed is an alternative to heart transplantation for patients suffering from low cardiac output syndrome.
It has recently been proposed to implant a dual-chamber pacemaker in patients suffering from low cardiac output syndrome and to configure such pacemaker to provide PV or AV pacing. During PV or AV pacing, the pacemaker delivers a V-pulse to the ventricles a programmed delay after the occurrence of an atrial event, which atrial event could be either the occurrence of a P-wave or the delivery of an A-pulse. Advantageously, by forcing a ventricular contraction prior to the occurrence of an R-wave, i.e., prior to natural depolarization of the ventricles, the cardiac output of patients suffering from cardiomyopathies may be significantly improved. Such improvement appears to result because the ventricular stimulus--a V-pulse delivered by the pacemaker--is applied to the ventricular tissue at a different cardiac location (at the location of the ventricular lead tip electrode, which location is usually in the apex of the right ventricle) than is the natural stimulus when received through the SA node.
PV or AV pacing is only effective, however, when the V-pulse is delivered to the ventricular tissue before the occurrence of an R-wave, i.e., before the ventricular tissue depolarizes. As soon as the ventricular tissue depolarizes, it becomes refractory, and will not respond to a V-pulse, until such time as it repolarizes. It is thus necessary, if AV or PV pacing is to be used, to set the AV (or PV) interval of the pacemaker to a value that is less than the patient's normal conduction time. Unfortunately, heretofore, this requirement has forced the AV (or PV) interval to be set to very short values, i.e., between 80 and 120 msec, because during exercise (or other periods of physical activity or physiological stress) the patient's native conduction time may shorten significantly. Thus, in order to guarantee that the pacemaker will always pace the ventricles, i.e., in order to assure that the V-pulse is delivered to the ventricular tissue at a time when it is not refractory, the AV (or PV) interval must be set to an interval that is shorter than any native conduction interval that might exist in any given patient at any given time.
Disadvantageously, setting a very short programmed AV (or PV) interval may adversely affect cardiac output because it may force ventricular contraction well before the ventricles have had sufficient time to be filled with blood from the atrium. Thus, what is needed for patients suffering from a cardiomyopathy is a pacemaker that paces the ventricles at a time in the cardiac cycle that is always less than the natural conduction time, i.e., at a time that is prior to the occurrence of an R-wave, but that is not so much less than the natural conduction time so as to adversely affect cardiac output. That is, what is needed is a pacemaker that automatically sets its internally-generated AV and/or PV intervals to be just short of the patient's native conduction time, thereby assuring that the AV (or PV) interval is sufficiently long to allow the blood to physically move from the atrium to the ventricles; yet remains sufficiently short to always be less than the patient's native conduction time, thereby assuring that the V-pulse is not delivered when the ventricular tissue is refractory.
The present invention advantageously addresses the above and other needs. See Applicant's copending application, filed concurrently herewith, entitled DUAL-CHAMBER IMPLANTABLE PACEMAKER HAVING AN ADAPTIVE AV INTERVAL THAT PREVENTS VENTRICULAR FUSION BEATS, Ser. No. 07/976,153, Attorney Docket No. GR 92P 7968, which application is incorporated herein by reference.